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Y2 CARDIORESP > Structural heart Disease > Flashcards

Structural heart Disease Flashcards

1
Q

What are the six main congenital structural heart diseases?

A

Atrial septal defect
Ventricular septal defect
Coarction of aorta
Patent Foramen ovale
Patent ductus arteriousus
Tetralogy of Fallot (TOF)

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2
Q

What is atrial septal defect?

A

A hole in the septum that divides the atria

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3
Q

What is ventricular septal defect?

A

A hole in the septum between the ventricles

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4
Q

What is tetralogy of fallot?

A

A combination of: ventricular septal defect, pulmonary stenosis, aortic valve sitting directly of top of ventricular septal defect and ventricular hypertrophy

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5
Q

What is coarctation of aorta?

A

A part of the aorta is narrower than usual which can block normal blood flow and back up flow into the left ventricle of the heart

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6
Q

What are the four types of valvular defects?

A

Aortic stenosis, aortic regurgitation, mitral stenosis and mitral regurgitation

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7
Q

What is the most common valvular disease in the US and Europe?

A

Aortic stenosis

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8
Q

What disease precedes aortic stenosis?

A

Aortic sclerosis (aortic valve thickening without flow limitation)

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9
Q

How is aortic stenosis often detected?

A

Presence of an early-peaking, systolic ejection murmur and confirmed by echocardiography

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10
Q

What risk factors are associated with aortic stenosis?

A

Hypertension, LDL levels, elevated Crp, congenital bicuspid valves, chronic kidney disease, radiotherapy, older age

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11
Q

what are the causes of aortic stenosis? (3)

A

Rheumatic heart disease, congenital heart disease, calcium build up

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12
Q

What is the pathophysiology behind aortic stenosis?

A

Long standing pressure overload leading to left ventricular hypertrophy
Increased after load as ventricle maintains a normal wall stress despite the pressure overload produced by stenosis.
Stenosis worsen so adaptive mechanism fells and left ventricular wall stress increases..
Causes systolic function decline

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13
Q

How is the severity of aortic stenosis determined?

A

By calculating speed of blood flow through the valve.
Severe if >4m/s. Done by trans-thoracic-echocardiogram

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14
Q

What is the aortic regurgitation?

A

Diastolic leakage of blood from the aorta into the left ventricle due to incompetence of valve resulting in intrinsic valve disease or dilation of aortic root

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15
Q

Which is the least common out of: aortic stenosis, mitral regurgitation and aortic regurgitation

A

Aortic regurgitation

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16
Q

What what are the congenital and acquired causes of aortic regurgitation?

A

Rheumatic heart disease, infective endocarditis, aortic valve stenosis, congenital heart defects, congenital bicuspid valves

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17
Q

What are the causes of aortic root dilation that precede aortic regurgitation?

A

Marfans syndrome
Connective tissue disease/ collagen vascular diseases
Idiopathic
Ankylosing spondilytis
Trauma

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18
Q

Is aortic regurgitation chronic or acute?

A

Can be both: chronic culminating into congestive cardiac failure.
Acute: medical emergency presenting with sudden onset of pulmonary oedema and hypotension or cardiogenic shock

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19
Q

What is the pathophysiology behind acute aortic regurgitation?

A

Increased blood volume in LV during systole leading to an increase in end diastolic pressure and pulmonary venous pressure, leading to dyspnoea and pulmonary oedema-> heart failure -> cardiogenic shock

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20
Q

What is the pathophysiology behind chronic aortic regurgitation?

A

Gradual increase in LV volume, LV enlargement and hypertrophy.
In early stages ejection fraction normal, after some time falls and LV end systolic volume rises
Eventually LV dyspnoea and lower coronary perfusion, ischaemia, necrosis and apoptosis

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21
Q

Outline the presentation of acute aortic regurgitation?

A

Cardiogenic shock, tachycardia, cyanosis, pulmonary oedema and Austin flint murmur

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22
Q

Outline the presentation of chronic aortic regurgitation

A

Wide pulse pressure, corridor, pistol shot pulse

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23
Q

What investigations are done in the diagnosis of aortic regurgitation?

A

Transthoracic echocardiography
Chest x ray
Cardiac catheterisation
Cardiac MRI/CT scan

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24
Q

What are the management options for acute aortic regurgitation?

A

Ionotropes/ vasodilators and valve replacement/repair

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25
Q

What are the Management options for chronic asymptomatic and chronic symptomatic aortic regurgitation?

A

Chronic asymptomatic: if LV function is normal can be managed by drugs
Chronic symptomatic: valve replacement with adjunct vasodilator therapy

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26
Q

What preventative measure can be put in place to avoid aortic regurgitation?

A

Treatment of rheumatic fever and infective endocarditis

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27
Q

What is mitral stenosis

A

Narrowing of the valve between the left aorta and ventricle

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28
Q

What are the causes of mitral stenosis?

A

Rheumatic fever, carcinoid syndrome, use of serotonergic drugs, SLE, mitral annular calcification due to aging, whipple disease

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29
Q

Outline the pathophysiology behind mitral stenosis

A

Exercise/ tachycardia result in exertional dyspnoea due to increased left atrial pressure
Severe mitral stenosis leads to increase in left atrial pressure, transudation of fluid into the lung interstitium leading to dyspnoea at rest or exertion.
Pulmonary hypertension may develop as a result of it

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30
Q

What are the long term effects of mitral stenosis?

A

Increased pressure in LA.
Increased strain causes dilation of LA
Proarrythmogenic

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31
Q

How is mitral stenosis detected?

A

Heard during diastole, trickier to recognise

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32
Q

What happens when you have both mitral and aortic stenosis on the left side?

A

Increased afterload on left ventricle, has to work harder to pump blood, contraction is less effective, abnormal remodelling, left ventricular hypertrophy

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33
Q

What are the causes of mitral regurgitation?

A

Rheumatic fever, mitral valve prolapse, infective endocarditis, if LV dilates too much -> leaking of valve

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34
Q

What are the immediate effects associated with mitral regurgitation?

A

Regurgitation of blood when LV contracts, less cardiac output, less blood being pumped out of aorta, less volume of blood reaching body

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35
Q

Why is it essential that mitral regurgitation is treated?

A

Can lead to death by heart failure, become congested and may need appropriate medication, diuretics. Important to treat and replace valve when severe

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36
Q

How is mitral regurgitation detected?

A

Systolic murmur

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37
Q

How is progressive asymptomatic mitral stenosis managed?

A

No therapy required

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38
Q

How is severe asymptomatic mitral stenosis managed?

A

No therapy generally required adjuvant balloon valvotomy

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39
Q

What are the management options for severe symptomatic mitral stenosis?

A

Diuretic, balloon valvotomy, valve replacement and repair adjuvant beta blockers

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40
Q

How is acute mitral regurgitation managed?

A

Emergency surgery adjunct. Preoperative diuretics. adjunct intra-aortic balloon counterpulsation

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41
Q

What are the management options for chronic asymptomatic mitral regurgitation?

A

ACE inhibitors, beta blockers if left ventricular ejection fraction is less than 60%. Surgery

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42
Q

What are the management options for chronic symptomatic mitral regurgitation?

A

Surgery plus medical treatment. If left ventricular ejection fraction is less than 30% intra-aortic balloon counterpulsation

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43
Q

What is a cardiomyopathy?

A

A disease of the heart muscle that makes it harder for heart to pump blood to the rest of the body

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44
Q

What are the three main types of cardiomyopathy?

A

Dilated, hypertrophic and restrictive

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45
Q

What percentages of the causes of dilated cardiomyopathy are familial?

A

25%

46
Q

What are the familial causes of dilated cardiomyopathy?

A

Primary without family history - idiopathic

47
Q

what are the secondary causes of dilated cardiomyopathy?

A

Heart valve disease, after child birth, thyroid disease, myocarditis, alcoholism, autoimmune disorders, ingestion of drugs, mitochondrial disorders

48
Q

What is dilated cardiomyopathy?

A

Causes heart chambers to thin and stretch, growing larger

49
Q

What is hypertrophic cardiomyopathy?

A

Heart muscle cells enlarge and walls of heart chamber thicken

50
Q

What is restrictive cardiomyopathy?

A

Fatty fibrous tissue replaces normal heart muscle

51
Q

Outline the abnormal physiology of dilated cardiomyopathy

A

Enlargement of the left ventricle
•lower ejection fraction and increase in the ventricular wall stress and end systolic volumes.
• Early compensatory mechanisms include an increase in heart rate and tone of the peripheral vascular system.
•neurohumoral activation of the renin-angiotensin aldosterone system and an increase in circulating levels of catecholamines.
•levels of natriuretic peptides are also increased.
•Eventually these compensatory mechanisms become overwhelmed and the heart fails.

52
Q

How does dilated cardiomyopathy usually present?

A

Dyspnoea, displaced apex beat, S3 or systolic murmur
fatigue,
angina,
pulmonary congestion
low cardiac output

53
Q

What investigations are conducted to confirm dilated cardiomyopathy?

A

Genetic Testing
•Viral serology
•ECG
•Chest X ray
•Cardiac catheterisation
•Cardiac MRI/CT Scan
•Exercise stress test
•Echocardiography

54
Q

What diet modifications are needed to manage dilated cardiomyopathy?

A

Fluid and Na+ restriction

55
Q

How do we treat the underlying causes of dilated cardiomyopathy?

A

Immunosuppressant for sarcoidosis and myocarditis
Phlebotomy for haemochromatosis

56
Q

How do we manage the symptoms of heart failure associated with dilated cardiomyopathy?

A

ACEi, beta-blockers with addition of diuretics and angiotensin2 receptor antagonists

57
Q

In the treatment of the symptoms of heart failure associated with dilated cardiomyopathy, what should be done if following ACEi and beta-blockers, the patient develops a cough, hypotension and/or renal dysfunction?

A

Lower dose of ACEi

58
Q

If medical treatment (ACEi and beta-blockers with diuretics and angiotensin2 receptor antagonists) is ineffective in treating the symptoms of heart failure associated with dilated cardiomyopathy, what is the next step in management?

A

For a surgical candidate: LVAD or orthotopic heart transplantation
For a non-surgical candidate: possible LVAD or optimisation of medical management

59
Q

What is given to manage the arrhythmias associated with dilated cardiomyopathy?

A

Amiodarone, defoteilide

60
Q

What is given to prevent thrombo-embolic events associated with heart failure in someone with a HX of TE, severe systolic dysfunction or ventricular dilatation?

A

Anticoagulants such as warfarin

61
Q

What are the characteristics of cardiac hypertrophy?

A

May have abnormal ECG, left ventricles abnormally thickened
May have abnormal thickening in wall in between chambers
can obstruct blood flow through the aorta
Murmur can mimic aortic stenosis, heard in systole ‘ejection systolic murmur’

62
Q

A dilated heart has what affect on contractility?
What can cause this?

A

Poor contractility (law of LaPlace)

Stress induced, peripartum, sarcoidosis, immune diseases, ischaemic etiology

63
Q

What is needed to be done in investigating a dilated heart to diagnose the cause and manage the patient?

A

Angiogram
Also family screening

64
Q

What is arrythmogenic right ventricular cardiomyopathy?

A

group of disorders which can lead to abnormal ventricular arrythmia -> abnormal contraction, impaired cardiac output

65
Q

What are the affects of infiltration of fat into the heart?

A

Abnormal diameter and function, dilated
Not pumping effectively, can also affect LV as intrinsically linked
May not be symptomatic
Can cause ventricular tachycardia -> lead to sudden death (must check for family history of this)

66
Q

How are heart valve lesions treated?

A

By replacing the valve before the patient becomes symptomatic or before the heart decompensates

67
Q

What is the hallmark of hypertrophic cardiomyopathy?

A

Hypertrophy that is inappropriate, often asymmetrical, and occurs in the absence of an obvious hypertrophy stimulus

68
Q

In hypertrophic cardiomyopathy, where is the most frequent site of hypertrophy?

A

Interventricular septum, which results in an obstruction of flow through the left ventricular outflow tract

69
Q

Outline the abnormal physiology associated with hypertrophic cardiomyopathy

A

Most patients with HCM have abnormal diastolic function, which impairs ventricular filling and increases filling pressure, despite a normal or small ventricular cavity.
These patients have abnormal calcium kinetics and subendocardial ischemia, which are related to the profound hypertrophy and myopathic process.

70
Q

How does hypertrophic cardiomyopathy usually present?

A

Sudden cardiac death Double carotid artery impulse, S3 gallop,
Syncope ejection systolic murmur
Presyncope
Congestive heart failure
Dizziness
Palpitations
Angina

71
Q

What investigations are conducted to confirm hypertrophic cardiomyopathy?

A

Hemoglobin level: Anemia exacerbates chest pain and dyspnea
•Brain natriuretic peptide (BNP), troponin T levels: Elevated BNP, NT-proBNP, and troponin T levels are associated with a higher risk of cardiovascular events, heart failure, and death
•Echocardiography
•Chest Xray
•Cardiac MRI

72
Q

What is the first line of treatment in the management of hypertrophic cardiomyopathy?

A

beta-blockers

73
Q

What is restrictive cardiomyopathy?

A

Increased stiffness of the myocardium

74
Q

Outline the abnormal physiology of restrictive cardiomyopathy

A

Increased stiffness of the myocardium causes ventricular pressures to rise precipitously with small increases in volume.

Thus, accentuated filling occurs in early diastole and terminates abruptly at the end of the rapid filling phase.

Patients typically have reduced compliance (increased diastolic stiffness), and the left ventricle cannot fill adequately at normal filling pressures

Reduced left ventricular filling volume leads to a reduced cardiac output.

75
Q

How does restrictive cardiomyopathy usually present?

A

comfortable in the sitting position because of fluid in the abdomen or lungs, and they frequently have ascites and pitting edema of the lower extremities.

•The liver is usually enlarged and full of fluid, which may be painful.

•Weight loss and cardiac cachexia are not uncommon.

•Easy bruising, periorbital purpura, macroglossia, and other systemic findings, such as carpal tunnel syndrome, should be an indication for the clinician to consider amyloidosis.
•Increased jugular venous pressure is present.

•The pulse volume is decreased, consistent with decreased stroke volume and cardiac output.

76
Q

What investigations are conducted to confirm restrictive cardiomyopathy?

A

CBC, Serology, Amylodosis check, Chest Xray ,ECG ,Echocardiography, Catheterisation, MRI/Biopsy

77
Q

Outline the management pathway for restrictive cardiomyopathy

A

Heart failure medication
Guideline-directed medical therapy for heart failure, including angiotensin-converting enzyme inhibitors or angiotensin receptor II blockers, diuretics and aldosterone inhibitors should be initiated in patients with reduced LV

Antiarrhythmic Therapy

Immunosuppression- Steroids

Pacemaker

Cardiac transplantation

78
Q

Outline the seven phases of the cardiac cycle

A

Atrial systole - blood ejected into ventricles, AV valve open
Isovolumetric contraction - all valves closed, ventricles contract
Rapid ejection - pressure in ventricles higher than post semi lunar valve pressure, blood ejected quickly
Slow ejection - pressure gradient falls, blood ejection slower
Isovolumetric relaxation
Rapid passive filling
Slow passive filling

79
Q

Which phase of the cardiac cycle is first impaired in heart failure?

A

Isovolumetric relaxation

80
Q

What drug should be administered as soon as possible to minimise damage to the heart in heart failure?

A

Beta-blockers

81
Q

Cardiac stroke volume is determined by what two factors?

A

Energy of contraction (preload) - starlings law of the heart, cardiac contractility
Arterial pressure (afterload)

82
Q

Outline Starlings law of the heart

A

A length-tension relationship describing how stretch of myocardium in diastole enhances contractile energy created

83
Q

In Starlings law of the heart, how does a stressing myocardium cause negative effects on contractile energy?

A

Reduces overlap of myocardial fibres, decreased interference causes negative effect on contractile energy

84
Q

What is the slower effect of Starlings law of the heart?

A

Sub-cellular increase in calcium stores

85
Q

What is the anrep effect of Starlings law of the heart?

A

Increases force of contraction by increasing number of cross bridges formed

86
Q

What are the two factors that determine cardiac contractility?

A

Sympathetic tone - sympathetic nerve fibres supplying the myocardium
Adrenaline - increasing contractile force of myocardium

87
Q

What is the relationship between preload and hypovolemia?

A

If a patient is bleeding or dehydrated there will be less blood volume circulating so blood pressure falls and stroke volume increases this means there is less preload as there is less stretching of the myocardium to generate energy of contraction

88
Q

What is afterload?

A

Pressure in aorta, force per unit cross section area, opposes shortening of myocardium in isotonic manner

89
Q

how is afterload involved in hypertension?

A

Increased afterload impairs stroke volume, can get adverse effects such as negative remodelling - heart muscle thickens and pumps dysfunctionally

90
Q

What is the Law of LaPlace?

A

Translates internal diameter radius of a chamber to wall tension and internal pressure generated by chamber. Ie internal pressure generated inside a chamber is directly proportional to wall tension

91
Q

Per Law of LaPlace, internal pressure generated inside a chamber is inversely proportional to what?>

A

Radius of the chamber

92
Q

In pathological states (e.g. heart failure / dilated cardiomyopathy), why does contractility fall (Law of LaPlace)

A

Radius of chamber increases meaning the chamber is unable to generate effective internal pressure

93
Q

What is the equation that describes the Law of LaPlace?

A

P=2T/r and P=2Sw/r
P = pressure
r = radius
T = tension
Sw = wall stress x wall thickness
Increase thickness = increase pressure generated

94
Q

In athletic hearts what changes can be seen to maintain BP needed?

A

The muscle is strengthened to increase contractile force - chamber with small radius, bigger internal force due to wall tension

95
Q

Which valve closes during ventricular filling?

A

Mitral valve

96
Q

Which valve opens during late isovolumetric contraction?

A

Aortic valve

97
Q

Which valve closes following ejection?

A

Aortic valve

98
Q

Which valve opens following isovolumetric relaxation ?

A

Mitral valve

99
Q

What are the two possible types of valvular lesions?

A

Stenosis lesions - narrowing
Dilatation - regurgitation lesions

100
Q

On which side of the heart are valvular lesions more significant and what do they lead to?

A

Left sided valvular lesions are more clinically significant, lead to mitral and aortic stenosis

101
Q

How is aortic stenosis detected?

A

Heart murmuring during systole

102
Q

How is mitral regurgitation detected?

A

Systolic murmur

103
Q

why is mitral regurgitation important to treat?

A

Can die of heart failure, become congested so need appropriate medication - diuretics
Important to treat and replace valve when severe

104
Q

How is aortic regurgitation detected?

A

Diastolic murmur

105
Q

What are the characteristics of cardiac hypertrophy?

A

May have abnormal ECG, left ventricles abnormally thickened
May have abnormal thickening in wall in between chambers - can obstruct blood flow through the aorta, murmur can mimic aortic stenosis, heard in systole ‘ ejection systolic murmur;

106
Q

A dilated heart leads to poor contractility, this can be caused by:

A

Stress induced
Infectious causes
Peripartum
Sarcoidosis
Immune disease
Ischaemic aetiology

107
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

A group of discovers which can lead to abnormal ventricular arrhythmia - abnormal contraction, impaired cardiac output

108
Q

What can infiltration of fat into the heart cause?

A

Abnormal diameter and function, dilated
Not pumping effectively, can also affect LV as intrinsically linked
May not be symptomatic
Can cause ventricular tachycardia and lead to sudden death (must check for family history of this)

109
Q

How are valve lesions treated?

A

By replacing the valve before the patient becomes symptomatic or before the heart decompensates

110
Q

What is cardiogenic shock?

A

Impairment of cardiac systolic function resulting in reduced CO
End organ dysfunction as not getting vital blood supply from stroke volume of heart
Receiving less oxygen and glucose for sufficient aerobic respiration
81% due to STEMI

111
Q

What are the treatment options for cardiogenic shock?

A

Keep transthoracic echocardiogram at bedside to see if ventricles aren’t pumping
Early coronary angiography to visualise narrow vessels
Urgent percutaneous cornonary intervention (PCI) - stents to open up narrow arteries causing the MI, or urgent coronary artery bypass grafting

Y2 CARDIORESP (15 decks)

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